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Journal articles on the topic 'Checkpoint in G2 / G2 checkpoint'

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Published: 9 March 2023

Last updated: 19 July 2025

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1

Xu, Bo, Seong-Tae Kim, Dae-Sik Lim, and Michael B. Kastan. "Two Molecularly Distinct G2/M Checkpoints Are Induced by Ionizing Irradiation." Molecular and Cellular Biology 22, no. 4 (2002): 1049–59. http://dx.doi.org/10.1128/mcb.22.4.1049-1059.2002.

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ABSTRACT Cell cycle checkpoints are among the multiple mechanisms that eukaryotic cells possess to maintain genomic integrity and minimize tumorigenesis. Ionizing irradiation (IR) induces measurable arrests in the G1, S, and G2 phases of the mammalian cell cycle, and the ATM (ataxia telangiectasia mutated) protein plays a role in initiating checkpoint pathways in all three of these cell cycle phases. However, cells lacking ATM function exhibit both a defective G2 checkpoint and a prolonged G2 arrest after IR, suggesting the existence of different types of G2 arrest. Two molecularly distinct G2

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2

Qiu, Ling, Andrew Burgess, David P. Fairlie, Helen Leonard, Peter G. Parsons, and Brian G. Gabrielli. "Histone Deacetylase Inhibitors Trigger a G2 Checkpoint in Normal Cells That Is Defective in Tumor Cells." Molecular Biology of the Cell 11, no. 6 (2000): 2069–83. http://dx.doi.org/10.1091/mbc.11.6.2069.

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Important aspects of cell cycle regulation are the checkpoints, which respond to a variety of cellular stresses to inhibit cell cycle progression and act as protective mechanisms to ensure genomic integrity. An increasing number of tumor suppressors are being demonstrated to have roles in checkpoint mechanisms, implying that checkpoint dysfunction is likely to be a common feature of cancers. Here we report that histone deacetylase inhibitors, in particular azelaic bishydroxamic acid, triggers a G2 phase cell cycle checkpoint response in normal human cells, and this checkpoint is defective in a

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Soni, Aashish, Xiaolu Duan, Martin Stuschke, and George Iliakis. "ATR Contributes More Than ATM in Intra-S-Phase Checkpoint Activation after IR, and DNA-PKcs Facilitates Recovery: Evidence for Modular Integration of ATM/ATR/DNA-PKcs Functions." International Journal of Molecular Sciences 23, no. 14 (2022): 7506. http://dx.doi.org/10.3390/ijms23147506.

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The intra-S-phase checkpoint was among the first reported cell cycle checkpoints in mammalian cells. It transiently slows down the rate of DNA replication after DNA damage to facilitate repair and thus prevents genomic instability. The ionizing radiation (IR)-induced intra-S-phase checkpoint in mammalian cells is thought to be mainly dependent upon the kinase activity of ATM. Defects in the intra-S-phase checkpoint result in radio-resistant DNA synthesis (RDS), which promotes genomic instability. ATM belongs to the PI3K kinase family along with ATR and DNA-PKcs. ATR has been shown to be the ke

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4

Osman, Fekret, Irina R. Tsaneva, Matthew C. Whitby, and Claudette L. Doe. "UV Irradiation Causes the Loss of Viable Mitotic Recombinants in Schizosaccharomyces pombe Cells Lacking the G2/M DNA Damage Checkpoint." Genetics 160, no. 3 (2002): 891–908. http://dx.doi.org/10.1093/genetics/160.3.891.

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Abstract Elevated mitotic recombination and cell cycle delays are two of the cellular responses to UV-induced DNA damage. Cell cycle delays in response to DNA damage are mediated via checkpoint proteins. Two distinct DNA damage checkpoints have been characterized in Schizosaccharomyces pombe: an intra-S-phase checkpoint slows replication and a G2/M checkpoint stops cells passing from G2 into mitosis. In this study we have sought to determine whether UV damage-induced mitotic intrachromosomal recombination relies on damage-induced cell cycle delays. The spontaneous and UV-induced recombination

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5

Li, Fanghua, Emil Mladenov, Rositsa Dueva, Martin Stuschke, Beate Timmermann, and George Iliakis. "Shift in G1-Checkpoint from ATM-Alone to a Cooperative ATM Plus ATR Regulation with Increasing Dose of Radiation." Cells 11, no. 1 (2021): 63. http://dx.doi.org/10.3390/cells11010063.

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The current view of the involvement of PI3-kinases in checkpoint responses after DNA damage is that ATM is the key regulator of G1-, S- or G2-phase checkpoints, that ATR is only partly involved in the regulation of S- and G2-phase checkpoints and that DNA-PKcs is not involved in checkpoint regulation. However, further analysis of the contributions of these kinases to checkpoint responses in cells exposed to ionizing radiation (IR) recently uncovered striking integrations and interplays among ATM, ATR and DNA-PKcs that adapt not only to the phase of the cell cycle in which cells are irradiated,

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6

Xu, Zhiheng, and David Norris. "The SFP1 Gene Product of Saccharomyces cerevisiae Regulates G2/M Transitions During the Mitotic Cell Cycle and DNA-Damage Response." Genetics 150, no. 4 (1998): 1419–28. http://dx.doi.org/10.1093/genetics/150.4.1419.

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Abstract In eukaryotic cells, checkpoint pathways arrest cell-cycle progression if a particular event has failed to complete appropriately or if an important intracellular structure is defective or damaged. Saccharomyces cerevisiae strains that lack the SFP1 gene fail to arrest at the G2 DNA-damage checkpoint in response to genomic injury, but maintain their ability to arrest at the replication and spindle-assembly checkpoints. sfp1Δ mutants are characterized by a premature entrance into mitosis during a normal (undamaged) cell cycle, while strains that overexpress Sfp1p exhibit delays in G2.

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7

Xu, Bo, Seong-tae Kim, and Michael B. Kastan. "Involvement of Brca1 in S-Phase and G2-Phase Checkpoints after Ionizing Irradiation." Molecular and Cellular Biology 21, no. 10 (2001): 3445–50. http://dx.doi.org/10.1128/mcb.21.10.3445-3450.2001.

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ABSTRACT Cell cycle arrests in the G1, S, and G2phases occur in mammalian cells after ionizing irradiation and appear to protect cells from permanent genetic damage and transformation. Though Brca1 clearly participates in cellular responses to ionizing radiation (IR), conflicting conclusions have been drawn about whether Brca1 plays a direct role in cell cycle checkpoints. Normal Nbs1 function is required for the IR-induced S-phase checkpoint, but whether Nbs1 has a definitive role in the G2/M checkpoint has not been established. Here we show that Atm and Brca1 are required for both the S-phas

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8

Dhar, Sonu, Jeremy A. Squire, M. Prakash Hande, Raymund J. Wellinger та Tej K. Pandita. "Inactivation of 14-3-3ς Influences Telomere Behavior and Ionizing Radiation-Induced Chromosomal Instability". Molecular and Cellular Biology 20, № 20 (2000): 7764–72. http://dx.doi.org/10.1128/mcb.20.20.7764-7772.2000.

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ABSTRACT Telomeres are complexes of repetitive DNA sequences and proteins constituting the ends of linear eukaryotic chromosomes. While these structures are thought to be associated with the nuclear matrix, they appear to be released from this matrix at the time when the cells exit from G2 and enter M phase. Checkpoints maintain the order and fidelity of the eukaryotic cell cycle, and defects in checkpoints contribute to genetic instability and cancer. The 14-3-3ς gene has been reported to be a checkpoint control gene, since it promotes G2 arrest following DNA damage. Here we demonstrate that

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9

Shigetomi, Hiroshi, Tamotsu Sudo, Keiji Shimada та ін. "Inhibition of Cell Death and Induction of G2 Arrest Accumulation in Human Ovarian Clear Cells by HNF-1β Transcription Factor: Chemosensitivity Is Regulated by Checkpoint Kinase CHK1". International Journal of Gynecologic Cancer 24, № 5 (2014): 838–43. http://dx.doi.org/10.1097/igc.0000000000000136.

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ObjectiveAppropriate cell cycle checkpoints are essential for the maintenance of normal cells and chemosensitivity of cancer cells. Clear cell adenocarcinoma (CCA) of the ovary is highly resistant to chemotherapy. Hepatocyte nuclear factor-1β (HNF-1β) is known to be overexpressed in CCA, but its role and clinical significance is unclear. We investigated the role of HNF-1β in regulation of the cell cycle in CCA.MethodsTo clarify the effects of HNF-1β on cell cycle checkpoints, we compared the cell cycle distribution and the expression of key proteins involved in CCA cells in which HNF-1β had be

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10

Rhind, Nicholas, and Paul Russell. "Roles of the Mitotic Inhibitors Wee1 and Mik1 in the G2 DNA Damage and Replication Checkpoints." Molecular and Cellular Biology 21, no. 5 (2001): 1499–508. http://dx.doi.org/10.1128/mcb.21.5.1499-1508.2001.

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ABSTRACT The G2 DNA damage and DNA replication checkpoints in many organisms act through the inhibitory phosphorylation of Cdc2 on tyrosine-15. This phosphorylation is catalyzed by the Wee1/Mik1 family of kinases. However, the in vivo role of these kinases in checkpoint regulation has been unclear. We show that, in the fission yeastSchizosaccharomyces pombe, Mik1 is a target of both checkpoints and that the regulation of Mik1 is, on its own, sufficient to delay mitosis in response to the checkpoints. Mik1 appears to have two roles in the DNA damage checkpoint; one in the establishment of the c

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11

Deckbar, Dorothee, Julie Birraux, Andrea Krempler, et al. "Chromosome breakage after G2 checkpoint release." Journal of Cell Biology 176, no. 6 (2007): 749–55. http://dx.doi.org/10.1083/jcb.200612047.

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DNA double-strand break (DSB) repair and checkpoint control represent distinct mechanisms to reduce chromosomal instability. Ataxia telangiectasia (A-T) cells have checkpoint arrest and DSB repair defects. We examine the efficiency and interplay of ATM's G2 checkpoint and repair functions. Artemis cells manifest a repair defect identical and epistatic to A-T but show proficient checkpoint responses. Only a few G2 cells enter mitosis within 4 h after irradiation with 1 Gy but manifest multiple chromosome breaks. Most checkpoint-proficient cells arrest at the G2/M checkpoint, with the length of

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12

Meng, Xiangbing, Jianling Bi, Yujun Li, et al. "AZD1775 Increases Sensitivity to Olaparib and Gemcitabine in Cancer Cells with p53 Mutations." Cancers 10, no. 5 (2018): 149. http://dx.doi.org/10.3390/cancers10050149.

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Tumor suppressor p53 is responsible for enforcing cell cycle checkpoints at G1/S and G2/M in response to DNA damage, thereby allowing both normal and tumor cells to repair DNA before entering S and M. However, tumor cells with absent or mutated p53 are able to activate alternative signaling pathways that maintain the G2/M checkpoint, which becomes uniquely critical for the survival of such tumor cells. We hypothesized that abrogation of the G2 checkpoint might preferentially sensitize p53-defective tumor cells to DNA-damaging agents and spare normal cells with intact p53 function. The tyrosine

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13

Naiki, Takahiro, Toshiyasu Shimomura, Tae Kondo, Kunihiro Matsumoto, and Katsunori Sugimoto. "Rfc5, in Cooperation with Rad24, Controls DNA Damage Checkpoints throughout the Cell Cycle inSaccharomyces cerevisiae." Molecular and Cellular Biology 20, no. 16 (2000): 5888–96. http://dx.doi.org/10.1128/mcb.20.16.5888-5896.2000.

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ABSTRACT RAD24 and RFC5 are required for DNA damage checkpoint control in the budding yeast Saccharomyces cerevisiae. Rad24 is structurally related to replication factor C (RFC) subunits and associates with RFC subunits Rfc2, Rfc3, Rfc4, and Rfc5. rad24Δ mutants are defective in all the G1-, S-, and G2/M-phase DNA damage checkpoints, whereas the rfc5-1 mutant is impaired only in the S-phase DNA damage checkpoint. Both the RFC subunits and Rad24 contain a consensus sequence for nucleoside triphosphate (NTP) binding. To determine whether the NTP-binding motif is important for Rad24 function, we

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Phong, Mark S., Robert D. Van Horn, Shuyu Li, Gregory Tucker-Kellogg, Uttam Surana, and Xiang S. Ye. "p38 Mitogen-Activated Protein Kinase Promotes Cell Survival in Response to DNA Damage but Is Not Required for the G2 DNA Damage Checkpoint in Human Cancer Cells." Molecular and Cellular Biology 30, no. 15 (2010): 3816–26. http://dx.doi.org/10.1128/mcb.00949-09.

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ABSTRACT p38 mitogen-activated protein kinase (MAPK) is rapidly activated by stresses and is believed to play an important role in the stress response. While Chk1 is known to mediate G2 DNA damage checkpoint control, p38 was also reported to have an essential function in this checkpoint control. Here, we have investigated further the roles of p38 and Chk1 in the G2 DNA damage checkpoint in cancer cells. We find that although p38 activation is strongly induced by DNA damage, its activity is not required for the G2 DNA damage checkpoint. In contrast, Chk1 kinase is responsible for the execution

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15

Kumar, Subodh, Srikanth Talluri, Mariateresa Fulciniti, Masood A. Shammas, and Nikhil C. Munshi. "Elevated APEX1 Disrupts G2/M Checkpoint, Contributing to Evolution and Survival of Myeloma Cells." Blood 126, no. 23 (2015): 2997. http://dx.doi.org/10.1182/blood.v126.23.2997.2997.

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Abstract Cell cycle checkpoints provide the cell with time to repair chromosomal DNA damage before its replication (G1) and also prior to its segregation (G2), thus ensuring integrity, maintenance and protection of genome. Although proper functioning of both checkpoints is essential, G2/M has a special significance as a potentially lethal double-strand break in DNA escape repair and persist from G2 into mitosis, it may recombine in G1 to produce gene rearrangements. Moreover, G2 is the phase where homologous recombination (HR) can utilize a sister chromatid as a template to provide error-free

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16

Lambert, Sarah, Sarah J. Mason, Louise J. Barber, et al. "Schizosaccharomyces pombe Checkpoint Response to DNA Interstrand Cross-Links." Molecular and Cellular Biology 23, no. 13 (2003): 4728–37. http://dx.doi.org/10.1128/mcb.23.13.4728-4737.2003.

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ABSTRACT Drugs that produce covalent interstrand cross-links (ICLs) in DNA remain central to the treatment of cancer, but the cell cycle checkpoints activated by ICLs have received little attention. We have used the fission yeast, Schizosaccharomyces pombe, to elucidate the checkpoint responses to the ICL-inducing anticancer drugs nitrogen mustard and mitomycin C. First we confirmed that the repair pathways acting on ICLs in this yeast are similar to those in the main organisms studied to date (Escherichia coli, budding yeast, and mammalian cells), principally nucleotide excision repair and ho

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17

De Souza, Colin P. C., Xiang S. Ye, and Stephen A. Osmani. "Checkpoint Defects Leading to Premature Mitosis Also Cause Endoreplication of DNA in Aspergillus nidulans." Molecular Biology of the Cell 10, no. 11 (1999): 3661–74. http://dx.doi.org/10.1091/mbc.10.11.3661.

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The G2 DNA damage and slowing of S-phase checkpoints over mitosis function through tyrosine phosphorylation of NIMXcdc2 inAspergillus nidulans. We demonstrate that breaking these checkpoints leads to a defective premature mitosis followed by dramatic rereplication of genomic DNA. Two additional checkpoint functions,uvsB and uvsD, also cause the rereplication phenotype after their mutation allows premature mitosis in the presence of low concentrations of hydroxyurea.uvsB is shown to encode a rad3/ATRhomologue, whereas uvsD displays homology torad26, which has only previously been identified inS

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18

O'Reilly, Michael A., Rhonda J. Staversky, Jacob N. Finkelstein, and Peter C. Keng. "Activation of the G2 cell cycle checkpoint enhances survival of epithelial cells exposed to hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 2 (2003): L368—L375. http://dx.doi.org/10.1152/ajplung.00299.2002.

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Reactive oxygen species produced during hyperoxia damage DNA, inhibit proliferation in G1- through p53-dependent activation of p21Cip1/WAF1/Sdi1, and kill cells. Because checkpoint activation protects cells from genotoxic stress, we investigated cell proliferation and survival of the murine type II epithelial cell line MLE15 during hyperoxia. These cells were chosen for study because they express Simian large and small-T antigens, which transform cells in part by disrupting the p53-dependent G1 checkpoint. Cell counts, 5-bromo-2′-deoxyuridine labeling, and flow cytometry revealed that hyperoxi

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Kawabe, Takumi. "G2 checkpoint abrogators as anticancer drugs." Molecular Cancer Therapeutics 3, no. 4 (2004): 513–19. http://dx.doi.org/10.1158/1535-7163.513.3.4.

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Abstract Many conventional anticancer treatments kill cells irrespective of whether they are normal or cancerous, so patients suffer from adverse side effects due to the loss of healthy cells. Anticancer insights derived from cell cycle research has given birth to the idea of cell cycle G2 checkpoint abrogation as a cancer cell specific therapy, based on the discovery that many cancer cells have a defective G1 checkpoint resulting in a dependence on the G2 checkpoint during cell replication. Damaged DNA in humans is detected by sensor proteins (such as hHUS1, hRAD1, hRAD9, hRAD17, and hRAD26)

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ARAI, MASAYOSHI, YUKIO KOIZUMI, HITOSHI SATO, et al. "Boromycin Abrogates Bleomycin-induced G2 Checkpoint." Journal of Antibiotics 57, no. 10 (2004): 662–68. http://dx.doi.org/10.7164/antibiotics.57.662.

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21

O’Connell, Matthew J., Nancy C. Walworth, and Antony M. Carr. "The G2-phase DNA-damage checkpoint." Trends in Cell Biology 10, no. 7 (2000): 296–303. http://dx.doi.org/10.1016/s0962-8924(00)01773-6.

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22

Campo, Del, R. Samaniego, J. F. Giménez-Abián, et al. "G2 checkpoint targets late replicating DNA." Biology of the Cell 95, no. 8 (2003): 521–26. http://dx.doi.org/10.1016/j.biolcel.2003.07.002.

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23

Rhind, Nicholas, and Paul Russell. "The Schizosaccharomyces pombe S-Phase Checkpoint Differentiates Between Different Types of DNA Damage." Genetics 149, no. 4 (1998): 1729–37. http://dx.doi.org/10.1093/genetics/149.4.1729.

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Abstract We have identified an S-phase DNA damage checkpoint in Schizosaccharomyces pombe. This checkpoint is dependent on Rad3, the S. pombe homolog of the mammalian ATM/ATR checkpoint proteins, and Cds1. Cds1 had previously been believed to be involved only in the replication checkpoint. The requirement of Cds1 in the DNA damage checkpoint suggests that Cds1 may be a general target of S-phase checkpoints. Unlike other checkpoints, the S. pombe S-phase DNA damage checkpoint discriminates between different types of damage. UV-irradiation, which causes base modification that can be repaired dur

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Forbes, Kristi Chrispell, Timothy Humphrey, and Tamar Enoch. "Suppressors of Cdc25p Overexpression Identify Two Pathways That Influence the G2/M Checkpoint in Fission Yeast." Genetics 150, no. 4 (1998): 1361–75. http://dx.doi.org/10.1093/genetics/150.4.1361.

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Abstract Checkpoints maintain the order of cell-cycle events. At G2/M, a checkpoint blocks mitosis in response to damaged or unreplicated DNA. There are significant differences in the checkpoint responses to damaged DNA and unreplicated DNA, although many of the same genes are involved in both responses. To identify new genes that function specifically in the DNA replication checkpoint pathway, we searched for high-copy suppressors of overproducer of Cdc25p (OPcdc25+), which lacks a DNA replication checkpoint. Two classes of suppressors were isolated. One class includes a new gene encoding a p

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Hayashi, S. "A Cdc2 dependent checkpoint maintains diploidy in Drosophila." Development 122, no. 4 (1996): 1051–58. http://dx.doi.org/10.1242/dev.122.4.1051.

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DNA replication in G2 does not normally occur due to the checkpoint control. To elucidate its mechanism, the functions of the escargot and Dmcdc2 genes of Drosophila were studied. When escargot function was eliminated, diploid imaginal cells that were arrested in G2 lost Cyclin A, a regulatory subunit of G2/M cdk, and entered an endocycle. escargot genetically interacted with Dmcdc2 which encodes a catalytic subunit of G2/M cdk. The mutant phenotypes of Dmcdc2 itself was similar to those of escargot: many diploid cells in imaginal discs, salivary glands and the central nervous system entered a

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Furnari, Beth, Alessandra Blasina, Michael N. Boddy, Clare H. McGowan, and Paul Russell. "Cdc25 Inhibited In Vivo and In Vitro by Checkpoint Kinases Cds1 and Chk1." Molecular Biology of the Cell 10, no. 4 (1999): 833–45. http://dx.doi.org/10.1091/mbc.10.4.833.

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In the fission yeast Schizosaccharomyces pombe, the protein kinase Cds1 is activated by the S–M replication checkpoint that prevents mitosis when DNA is incompletely replicated. Cds1 is proposed to regulate Wee1 and Mik1, two tyrosine kinases that inhibit the mitotic kinase Cdc2. Here, we present evidence from in vivo and in vitro studies, which indicates that Cds1 also inhibits Cdc25, the phosphatase that activates Cdc2. In an in vivo assay that measures the rate at which Cdc25 catalyzes mitosis, Cds1 contributed to a mitotic delay imposed by the S–M replication checkpoint. Cds1 also inhibite

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Yamada, Ayumi, Brad Duffy, Jennifer A. Perry, and Sally Kornbluth. "DNA replication checkpoint control of Wee1 stability by vertebrate Hsl7." Journal of Cell Biology 167, no. 5 (2004): 841–49. http://dx.doi.org/10.1083/jcb.200406048.

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G2/M checkpoints prevent mitotic entry upon DNA damage or replication inhibition by targeting the Cdc2 regulators Cdc25 and Wee1. Although Wee1 protein stability is regulated by DNA-responsive checkpoints, the vertebrate pathways controlling Wee1 degradation have not been elucidated. In budding yeast, stability of the Wee1 homologue, Swe1, is controlled by a regulatory module consisting of the proteins Hsl1 and Hsl7 (histone synthetic lethal 1 and 7), which are targeted by the morphogenesis checkpoint to prevent Swe1 degradation when budding is inhibited. We report here the identification of X

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Mikhailov, Alexei, Mio Shinohara, and Conly L. Rieder. "Topoisomerase II and histone deacetylase inhibitors delay the G2/M transition by triggering the p38 MAPK checkpoint pathway." Journal of Cell Biology 166, no. 4 (2004): 517–26. http://dx.doi.org/10.1083/jcb.200405167.

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When early prophase PtK1 or Indian muntjac cells are exposed to topoisomerase II (topo II) inhibitors that induce little if any DNA damage, they are delayed from entering mitosis. We show that this delay is overridden by inhibiting the p38, but not the ATM, kinase. Treating early prophase cells with hyperosmotic medium or a histone deacetylase inhibitor similarly delays entry into mitosis, and this delay can also be prevented by inhibiting p38. Together, these results reveal that agents or stresses that induce global changes in chromatin topology during G2 delay entry into mitosis, independent

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Orren, D. K., L. N. Petersen, and V. A. Bohr. "A UV-responsive G2 checkpoint in rodent cells." Molecular and Cellular Biology 15, no. 7 (1995): 3722–30. http://dx.doi.org/10.1128/mcb.15.7.3722.

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We have studied the effect of UV irradiation on the cell cycle progression of synchronized Chinese hamster ovary cells. Synchronization of cells in S or G2 phase was accomplished by the development of a novel protocol using mimosine, which blocks cell cycle progression at the G1/S boundary. After removal of mimosine, cells proceed synchronously through the S and G2 phases, allowing manipulation of cells at specific points in either phase. Synchronization of cells in G1 was achieved by release of cells after a period of serum starvation. Cells synchronized by these methods were UV irradiated at

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Passalaris, Tina M., Jennifer A. Benanti, Lindy Gewin, Tohru Kiyono, and Denise A. Galloway. "The G2 Checkpoint Is Maintained by Redundant Pathways." Molecular and Cellular Biology 19, no. 9 (1999): 5872–81. http://dx.doi.org/10.1128/mcb.19.9.5872.

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ABSTRACT While p53 activity is critical for a DNA damage-induced G1 checkpoint, its role in the G2 checkpoint has not been compelling because cells lacking p53 retain the ability to arrest in G2 following DNA damage. Comparison between normal human foreskin fibroblasts (HFFs) and HFFs in which p53 was eliminated by transduction with human papillomavirus type 16 E6 showed that treatment with adriamycin initiated arrest in G2 with active cyclin B/CDC2 kinase, regardless of p53 status. Both E6-transduced HFFs and control (LXSN)-transduced cells maintained a prolonged arrest in G2; however cells w

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Shibata, Atsushi, Olivia Barton, Angela T. Noon, et al. "Role of ATM and the Damage Response Mediator Proteins 53BP1 and MDC1 in the Maintenance of G2/M Checkpoint Arrest." Molecular and Cellular Biology 30, no. 13 (2010): 3371–83. http://dx.doi.org/10.1128/mcb.01644-09.

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ABSTRACT ATM-dependent initiation of the radiation-induced G2/M checkpoint arrest is well established. Recent results have shown that the majority of DNA double-strand breaks (DSBs) in G2 phase are repaired by DNA nonhomologous end joining (NHEJ), while ∼15% of DSBs are slowly repaired by homologous recombination. Here, we evaluate how the G2/M checkpoint is maintained in irradiated G2 cells, in light of our current understanding of G2 phase DSB repair. We show that ATM-dependent resection at a subset of DSBs leads to ATR-dependent Chk1 activation. ATR-Seckel syndrome cells, which fail to effi

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Balcer-Kubiczek, Elizabeth K., Mona Attarpour, Jian Z. Wang, and William F. Regine. "The Effect of Docetaxel (Taxotere®) on Human Gastric Cancer Cells Exhibiting Low-Dose Radiation Hypersensitivity." Clinical medicine. Oncology 2 (January 2008): CMO.S463. http://dx.doi.org/10.4137/cmo.s463.

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Low-dose radiation hypersensitivity (HRS) describes a phenomenon of excessive sensitivity to X ray doses <0.5 Gy. Docetaxel is a taxane shown to arrest cells in the G2/M phase of the cell cycle. Some previous studies suggested that HRS might result from the abrogation of the early G2 checkpoint arrest. First we tested whether HRS occurs in gastric cancer—derived cells, and whether pre-treatment of cells with low docetaxel concentrations can enhance the magnitude of HRS in gastric cancer cells. The results demonstrated HRS at ~0.3 Gy and the synergy between 0.3 Gy and docetaxel (3 nM for 24

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Flatt, Patricia M., Luo Jia Tang, Caroline D. Scatena, Suzanne T. Szak, and Jennifer A. Pietenpol. "p53 Regulation of G2 Checkpoint Is Retinoblastoma Protein Dependent." Molecular and Cellular Biology 20, no. 12 (2000): 4210–23. http://dx.doi.org/10.1128/mcb.20.12.4210-4223.2000.

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ABSTRACT In the present study, we investigated the role of p53 in G2 checkpoint function by determining the mechanism by which p53 prevents premature exit from G2 arrest after genotoxic stress. Using three cell model systems, each isogenic, we showed that either ectopic or endogenous p53 sustained a G2arrest activated by ionizing radiation or adriamycin. The mechanism was p21 and retinoblastoma protein (pRB) dependent and involved an initial inhibition of cyclin B1-Cdc2 activity and a secondary decrease in cyclin B1 and Cdc2 levels. Abrogation of p21 or pRB function in cells containing wild-ty

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Choudhuri, Tathagata, Subhash C. Verma, Ke Lan, Masanao Murakami, and Erle S. Robertson. "The ATM/ATR Signaling Effector Chk2 Is Targeted by Epstein-Barr Virus Nuclear Antigen 3C To Release the G2/M Cell Cycle Block." Journal of Virology 81, no. 12 (2007): 6718–30. http://dx.doi.org/10.1128/jvi.00053-07.

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ABSTRACT Epstein-Barr virus (EBV) infects most of the human population and persists in B lymphocytes for the lifetime of the host. The establishment of latent infection by EBV requires the expression of a unique repertoire of genes. The product of one of these viral genes, the EBV nuclear antigen 3C (EBNA3C), is essential for the growth transformation of primary B lymphocytes in vitro and can regulate the transcription of a number of viral and cellular genes important for the immortalization process. This study demonstrates an associated function of EBNA3C which involves the disruption of the

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Hasvold, Grete, Christin Lund-Andersen, Malin Lando, et al. "Hypoxia-induced alterations of G2 checkpoint regulators." Molecular Oncology 10, no. 5 (2016): 764–73. http://dx.doi.org/10.1016/j.molonc.2015.12.015.

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Calonge, Teresa M., and Matthew J. O’Connell. "Turning off the G2 DNA damage checkpoint." DNA Repair 7, no. 2 (2008): 136–40. http://dx.doi.org/10.1016/j.dnarep.2007.07.017.

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Trenkmann, Michelle. "A(TR) checkpoint for S/G2 transition." Nature Reviews Molecular Cell Biology 19, no. 11 (2018): 676–77. http://dx.doi.org/10.1038/s41580-018-0064-4.

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Nakagawa, Taku, Yoji Hayashita, Ken Maeno, et al. "Identification of Decatenation G2 Checkpoint Impairment Independently of DNA Damage G2 Checkpoint in Human Lung Cancer Cell Lines." Cancer Research 64, no. 14 (2004): 4826–32. http://dx.doi.org/10.1158/0008-5472.can-04-0871.

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Poggioli, George J., Roberta L. DeBiasi, Ryan Bickel, et al. "Reovirus-Induced Alterations in Gene Expression Related to Cell Cycle Regulation." Journal of Virology 76, no. 6 (2002): 2585–94. http://dx.doi.org/10.1128/jvi.76.6.2585-2594.2002.

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ABSTRACT Mammalian reovirus infection results in perturbation of host cell cycle progression. Since reovirus infection is known to activate cellular transcription factors, we investigated alterations in cell cycle-related gene expression following HEK293 cell infection by using the Affymetrix U95A microarray. Serotype 3 reovirus infection results in differential expression of 10 genes classified as encoding proteins that function at the G1-to-S transition, 11 genes classified as encoding proteins that function at G2-to-M transition, and 4 genes classified as encoding proteins that function at

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Paciotti, Vera, Michela Clerici, Maddalena Scotti, Giovanna Lucchini, and Maria Pia Longhese. "Characterization of mec1Kinase-Deficient Mutants and of New Hypomorphic mec1Alleles Impairing Subsets of the DNA Damage Response Pathway." Molecular and Cellular Biology 21, no. 12 (2001): 3913–25. http://dx.doi.org/10.1128/mcb.21.12.3913-3925.2001.

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ABSTRACT DNA damage checkpoints lead to the inhibition of cell cycle progression following DNA damage. The Saccharomyces cerevisiae Mec1 checkpoint protein, a phosphatidylinositol kinase-related protein, is required for transient cell cycle arrest in response to DNA damage or DNA replication defects. We show thatmec1 kinase-deficient (mec1kd) mutants are indistinguishable from mec1Δ cells, indicating that the Mec1 conserved kinase domain is required for all known Mec1 functions, including cell viability and proper DNA damage response. Mec1kd variants maintain the ability to physically interact

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Clerici, Michela, Veronica Baldo, Davide Mantiero, Francisca Lottersberger, Giovanna Lucchini, and Maria Pia Longhese. "A Tel1/MRX-Dependent Checkpoint Inhibits the Metaphase-to-Anaphase Transition after UV Irradiation in the Absence of Mec1." Molecular and Cellular Biology 24, no. 23 (2004): 10126–44. http://dx.doi.org/10.1128/mcb.24.23.10126-10144.2004.

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ABSTRACT In Saccharomyces cerevisiae, Mec1/ATR plays a primary role in sensing and transducing checkpoint signals in response to different types of DNA lesions, while the role of the Tel1/ATM kinase in DNA damage checkpoints is not as well defined. We found that UV irradiation in G1 in the absence of Mec1 activates a Tel1/MRX-dependent checkpoint, which specifically inhibits the metaphase-to-anaphase transition. Activation of this checkpoint leads to phosphorylation of the downstream checkpoint kinases Rad53 and Chk1, which are required for Tel1-dependent cell cycle arrest, and their adaptor R

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Yan, Tao, Anand B. Desai, James W. Jacobberger, R. Michael Sramkoski, Tamalette Loh, and Timothy J. Kinsella. "CHK1 and CHK2 are differentially involved in mismatch repair–mediated 6-thioguanine-induced cell cycle checkpoint responses." Molecular Cancer Therapeutics 3, no. 9 (2004): 1147–57. http://dx.doi.org/10.1158/1535-7163.1147.3.9.

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Abstract The DNA mismatch repair (MMR) system plays an important role in mediating a G2-M checkpoint arrest and subsequent cell death following treatment with a variety of chemotherapeutic agents. In this study, using 6-thioguanine (6-TG) as a mismatch-inducing drug, we examine the role of ataxia telangiectasia mutated (ATM)/CHK2 and ATM and Rad-3 related (ATR)/CHK1 signaling pathways in MMR-mediated cell cycle responses in MMR-proficient human colorectal cancer RKO cells. We show that, in response to 6-TG (3 μmol/L × 24 hours), activating phosphorylation of CHK1 at Ser317 [CHK1(pS317)] and CH

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Yu, Xiaochun, and Junjie Chen. "DNA Damage-Induced Cell Cycle Checkpoint Control Requires CtIP, a Phosphorylation-Dependent Binding Partner of BRCA1 C-Terminal Domains." Molecular and Cellular Biology 24, no. 21 (2004): 9478–86. http://dx.doi.org/10.1128/mcb.24.21.9478-9486.2004.

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ABSTRACT The BRCA1 C-terminal (BRCT) domain has recently been implicated as a phospho-protein binding domain. We demonstrate here that a CTBP-interacting protein CtIP interacts with BRCA1 BRCT domains in a phosphorylation-dependent manner. The CtIP/BRCA1 complex only exists in G2 phase and is required for DNA damage-induced Chk1 phosphorylation and the G2/M transition checkpoint. However, the CtIP/BRCA1 complex is not required for the damage-induced G2 accumulation checkpoint, which is controlled by a separate BRCA1/BACH1 complex. Taken together, these data not only implicate CtIP as a critica

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Saldivar, Joshua C., Stephan Hamperl, Michael J. Bocek, et al. "An intrinsic S/G2 checkpoint enforced by ATR." Science 361, no. 6404 (2018): 806–10. http://dx.doi.org/10.1126/science.aap9346.

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The cell cycle is strictly ordered to ensure faithful genome duplication and chromosome segregation. Control mechanisms establish this order by dictating when a cell transitions from one phase to the next. Much is known about the control of the G1/S, G2/M, and metaphase/anaphase transitions, but thus far, no control mechanism has been identified for the S/G2 transition. Here we show that cells transactivate the mitotic gene network as they exit the S phase through a CDK1 (cyclin-dependent kinase 1)–directed FOXM1 phosphorylation switch. During normal DNA replication, the checkpoint kinase ATR

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Zhu, Wenge, and Anindya Dutta. "An ATR- and BRCA1-Mediated Fanconi Anemia Pathway Is Required for Activating the G2/M Checkpoint and DNA Damage Repair upon Rereplication." Molecular and Cellular Biology 26, no. 12 (2006): 4601–11. http://dx.doi.org/10.1128/mcb.02141-05.

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ABSTRACT The timely assembly of prereplicative complexes at replication origins is tightly controlled to ensure that genomic DNA is replicated once per cell cycle. The loss of geminin, a DNA replication inhibitor, causes rereplication that activates a G2/M checkpoint in human cancer cells. Fanconi anemia (FA) is an autosomal recessive and X-linked disorder associated with cancer susceptibility. Here we show that rereplication activates the FA pathway both for the activation of a G2/M checkpoint and for repair processes, like recruitment of RAD51. Both ATR and BRCA1 are required to activate the

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Hirose, Yuichi, Makoto Katayama, David Stokoe, Daphne A. Haas-Kogan, Mitchel S. Berger, and Russell O. Pieper. "The p38 Mitogen-Activated Protein Kinase Pathway Links the DNA Mismatch Repair System to the G2 Checkpoint and to Resistance to Chemotherapeutic DNA-Methylating Agents." Molecular and Cellular Biology 23, no. 22 (2003): 8306–15. http://dx.doi.org/10.1128/mcb.23.22.8306-8315.2003.

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ABSTRACT Although human cells exposed to DNA-methylating agents undergo mismatch repair (MMR)-dependent G2 arrest, the basis for the linkage between MMR and the G2 checkpoint is unclear. We noted that mitogen-activated protein kinase p38α was activated in MMR-proficient human glioma cells exposed to the chemotherapeutic methylating agent temozolomide (TMZ) but not in paired cells made MMR deficient by expression of a short inhibitory RNA (siRNA) targeted to the MMR protein Mlh1. Furthermore, activation of p38α in MMR-proficient cells was associated with nuclear inactivation of the cell cycle r

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Terada, Yasuhiko, and Yuko Yasuda. "Human Immunodeficiency Virus Type 1 Vpr Induces G2 Checkpoint Activation by Interacting with the Splicing Factor SAP145." Molecular and Cellular Biology 26, no. 21 (2006): 8149–58. http://dx.doi.org/10.1128/mcb.01170-06.

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ABSTRACT Vpr, the viral protein R of human immunodeficiency virus type 1, induces G2 cell cycle arrest and apoptosis in mammalian cells via ATR (for “ataxia-telangiectasia-mediated and Rad3-related”) checkpoint activation. The expression of Vpr induces the formation of the γ-histone 2A variant X (H2AX) and breast cancer susceptibility protein 1 (BRCA1) nuclear foci, and a C-terminal domain is required for Vpr-induced ATR activation and its nuclear localization. However, the cellular target of Vpr, as well as the mechanism of G2 checkpoint activation, was unknown. Here we report that Vpr induce

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Luo, Daxian, Emil Mladenov, Aashish Soni, Martin Stuschke, and George Iliakis. "The p38/MK2 Pathway Functions as Chk1-Backup Downstream of ATM/ATR in G2-Checkpoint Activation in Cells Exposed to Ionizing Radiation." Cells 12, no. 10 (2023): 1387. http://dx.doi.org/10.3390/cells12101387.

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We have recently reported that in G2-phase cells (but not S-phase cells) sustaining low loads of DNA double-strand break (DSBs), ATM and ATR regulate the G2-checkpoint epistatically, with ATR at the output-node, interfacing with the cell cycle through Chk1. However, although inhibition of ATR nearly completely abrogated the checkpoint, inhibition of Chk1 using UCN-01 generated only partial responses. This suggested that additional kinases downstream of ATR were involved in the transmission of the signal to the cell cycle engine. Additionally, the broad spectrum of kinases inhibited by UCN-01 p

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Scott, Kenneth L., and Sharon E. Plon. "Loss of Sin3/Rpd3 Histone Deacetylase Restores the DNA Damage Response in Checkpoint-Deficient Strains of Saccharomyces cerevisiae." Molecular and Cellular Biology 23, no. 13 (2003): 4522–31. http://dx.doi.org/10.1128/mcb.23.13.4522-4531.2003.

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ABSTRACT We previously reported that expression of the human forkhead/winged helix transcription factor, CHES1 (checkpoint suppressor 1; FOXN3), suppresses sensitivity to DNA damage and restores damage-induced G2/M arrest in checkpoint-deficient strains of Saccharomyces cerevisiae. We find that a functional glutathione S-transferase-Ches1 fusion protein binds in vivo to Sin3, a component of the S. cerevisiae Sin3/Rpd3 histone deacetylase complex. Checkpoint mutant strains with SIN3 deleted show increased resistance to UV irradiation, which is not further enhanced by CHES1 expression. Conversel

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Liu, Shengqin, Brendan M. Byrne, Thomas N. Byrne, and Gregory G. Oakley. "Role of RPA Phosphorylation in the ATR-Dependent G2 Cell Cycle Checkpoint." Genes 14, no. 12 (2023): 2205. http://dx.doi.org/10.3390/genes14122205.

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Cells respond to DNA double-strand breaks by initiating DSB repair and ensuring a cell cycle checkpoint. The primary responder to DSB repair is non-homologous end joining, which is an error-prone repair pathway. However, when DSBs are generated after DNA replication in the G2 phase of the cell cycle, a second DSB repair pathway, homologous recombination, can come into action. Both ATM and ATR are important for DSB-induced DSB repair and checkpoint responses. One method of ATM and ATR working together is through the DNA end resection of DSBs. As a readout and marker of DNA end resection, RPA is

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